ArticleOxidative medicine and cellular longevity2021
Hydroxysafflor Yellow A Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Calcium Overload and Apoptosis.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- Advances in Chinese herbal medicine in modulating mitochondria to treat myocardial ischemia-reperfusion injury: a narrative review.Cardiovascular diagnosis and therapy · 2025Review
- Pharmacological actions and applications of safflower flavonoids.Frontiers in nutrition · 2025Review
- A Meta-Analysis of Randomized Controlled Trials (RCTs) Investigating the Efficacy and Safety of Acupuncture in Treating Myocardial Ischemia/Reperfusion (I/R) Injury.Cardiology research and practice · 2025Review
- Hydroxysafflor Yellow A Inhibits Pyroptosis and Protecting HUVECs from OGD/R via NLRP3/Caspase-1/GSDMD Pathway.Chinese journal of integrative medicine · 2024Article
- Transplantation of human endometrial perivascular stem cells with hydroxy saffron yellow A promotes uterine repair in rats.Stem cell research & therapy · 2024Article
- Natural L-type calcium channels antagonists from Chinese medicine.Chinese medicine · 2024Article
- An auxiliary strategy of partial least squares regression in pharmacokinetic/pharmacodynamic studies: A case of application of guhong injection in myocardial ischemia/reperfusion rats.Journal of food and drug analysis · 2024Article
- Exosomes-Mediated Signaling Pathway: A New Direction for Treatment of Organ Ischemia-Reperfusion Injury.Biomedicines · 2024Review
- Esketamine alleviates hypoxia/reoxygenation injury of cardiomyocytes by regulating TRPV1 expression and inhibiting intracellular CaClinics (Sao Paulo, Brazil) · 2024Article
- Article
- The traditional Chinese medicines treat chronic heart failure and their main bioactive constituents and mechanisms.Acta pharmaceutica Sinica. B · 2023Review
- The predictive value of the nomogram model of clinical risk factors for ischemia-reperfusion injury after primary percutaneous coronary intervention.Scientific reports · 2023Article
- Mechanism Repositioning Based on Integrative Pharmacology: Anti-Inflammatory Effect of Safflower in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2023Article
- Traditional chinese medicine in coronary microvascular disease.Frontiers in pharmacology · 2022Review
- The Improvement of Cardiac and Endothelial Functions of Xue-Fu-Zhu-Yu Decoction for Patients with Acute Coronary Syndrome: A Meta-Analysis of Randomized Controlled Trials.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Phosphorylated nuclear factor erythroid 2-related factor 2 promotes the secretion of C-C motif chemokine ligand 2 and the recruitment of M2 macrophages.Annals of translational medicine · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion injury (MI/RI) is an urgent problem with a great impact on health globally. However, its pathological mechanisms have not been fully elucidated. Hydroxysafflor yellow A (HSYA) has a protective effect against MI/RI. This study is aimed at further clarifying the relationship between HSYA cardioprotection and calcium overload as well as the underlying mechanisms. We verified the protective effect of HSYA on neonatal rat primary cardiomyocytes (NPCMs) and human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from hypoxia-reoxygenation (HR) injury. To explore the cardioprotective mechanism of HSYA, we employed calcium fluorescence, TUNEL assay, JC-1 staining, and western blotting. Finally, cardio-ECR and patch-clamp experiments were used to explain the regulation of L-type calcium channels (LTCC) in cardioprotection mediated by HSYA. The results showed that HSYA reduced the levels of myocardial enzymes and protected NPCMs from HR injury. HSYA also restored the contractile function of hiPSC-CMs and field potential signal abnormalities caused by HR and exerted a protective effect on cardiac function. Further, we demonstrated that HSYA protects cardiomyocytes from HR injury by decreasing mitochondrial membrane potential and inhibiting apoptosis and calcium overload. Patch-clamp results revealed that MI/RI caused a sharp increase in calcium currents, which was inhibited by pretreatment with HSYA. Furthermore, we found that HSYA restored contraction amplitude, beat rate, and field potential duration of hiPSC-CMs, which were disrupted by the LTCC agonist Bay-K8644. Patch-clamp experiments also showed that HSYA inhibits Bay-K8644-induced calcium current, with an effect similar to that of the LTCC inhibitor nisoldipine. Therefore, our data suggest that HSYA targets LTCC to inhibit calcium overload and apoptosis of cardiomyocytes, thereby exerting a cardioprotective effect and reducing MI/RI injury.
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